Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 강덕희 | - |
dc.date.accessioned | 2018-05-02T08:15:52Z | - |
dc.date.available | 2018-05-02T08:15:52Z | - |
dc.date.issued | 2003 | - |
dc.identifier.issn | 0194-911X | - |
dc.identifier.other | OAK-1498 | - |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/242831 | - |
dc.description.abstract | Previous studies have reported that uric acid stimulates vascular smooth muscle cell (VSMC) proliferation in vitro. We hypothesized that uric acid may also have direct proinflammatory effects on VSMCs. Crystal- and endotoxin-free uric acid was found to increase VSMC monocyte chemoattractant protein-1 (MCP-1) expression in a time- and dose-dependent manner, peaking at 24 hours. Increased mRNA and protein expression occurred as early as 3 hours after uric acid incubation and was partially dependent on posttranscriptional modification of MCP-1 mRNA. In addition, uric acid activated the transcription factors nuclear factor-κB and activator protein-1, as well as the MAPK signaling molecules ERK p44/42 and p38, and increased cyclooxygenase-2 (COX-2) mRNA expression. Inhibition of p38 (with SB 203580), ERK 44/42 (with UO126 or PD 98059), or COX-2 (with NS398) each significantly suppressed uric acid-induced MCP-1 expression at 24 hours, implicating these pathways in the response to uric acid. The ability of both N-acetyl-cysteine and diphenyleneionium (antioxidants) to inhibit uric acid-induced MCP-1 production suggested involvement of intracellular redox pathways. Uric acid regulates critical proinflammatory pathways in VSMCs, suggesting it may have a role in the vascular changes associated with hypertension and vascular disease. | - |
dc.language | English | - |
dc.title | Uric acid stimulates monocyte chemoattractant protein-1 production in vascular smooth muscle cells via mitogen-activated protein kinase and cyclooxygenase-2 | - |
dc.type | Article | - |
dc.relation.issue | 6 | - |
dc.relation.volume | 41 | - |
dc.relation.index | SCI | - |
dc.relation.index | SCIE | - |
dc.relation.index | SCOPUS | - |
dc.relation.startpage | 1287 | - |
dc.relation.lastpage | 1293 | - |
dc.relation.journaltitle | Hypertension | - |
dc.identifier.doi | 10.1161/01.HYP.0000072820.07472.3B | - |
dc.identifier.wosid | WOS:000183348400020 | - |
dc.identifier.scopusid | 2-s2.0-0038579374 | - |
dc.author.google | Kanellis J. | - |
dc.author.google | Watanabe S. | - |
dc.author.google | Li J.H. | - |
dc.author.google | Kang D.H. | - |
dc.author.google | Li P. | - |
dc.author.google | Nakagawa T. | - |
dc.author.google | Wamsley A. | - |
dc.author.google | Sheikh-Hamad D. | - |
dc.author.google | Lan H.Y. | - |
dc.author.google | Feng L. | - |
dc.author.google | Johnson R.J. | - |
dc.contributor.scopusid | 강덕희(17233695600) | - |
dc.date.modifydate | 20230210140157 | - |